ARFI imaging was observed to have no apparent histological damage to the placental tissue. Ex vivo placentas from the FGR group were significantly more firm. Moreover, Vs values and Z-scores of birthweight had a significant negative correlation. Additional investigations are needed about the utility of this method for the evaluation of placental function in vivo.
Background: Trophoblast cells, the functional components of the placenta, are derived from multipotent trophoblast stem (TS) cells. Results: SATB homeobox proteins regulate the TS cell stem state through up-regulation of a stem-specific transcription factor, EOMES, and inhibition of trophoblast differentiation. Conclusion: SATB proteins regulate TS cell development. Significance: Understanding TS cell biology is crucial to determining processes underlying placental development.
Abstract-The aim of this study was to investigate the role of neutrophil-derived reactive oxygen species on endothelial cell dysfunction in preeclampsia. We first assessed the correlation between nitrite and superoxide anion production in normal nonpregnant (nϭ10), normal pregnant (nϭ15), and preeclamptic women (nϭ12). We then examined neutrophil-mediated oxygen radical damage to human umbilical vein endothelial cells in vitro. Neutrophil superoxide release was measured by cytochrome C reduction; nitrite release was measured by the modified Griess reaction, and endothelial cell injury was measured by 51 Cr release. N-formyl-methionyl-leucyl-phenylalanine-stimulated superoxide release by neutrophils was significantly increased in women with preeclampsia compared with the other 2 groups. Nitrite release by neutrophils was significantly decreased in preeclampsia compared with normal pregnancy. When neutrophils were pretreated with superoxide dismutase, nitrite release by neutrophils did not differ between normal pregnancy and preeclampsia, suggesting that excess superoxide anion in preeclampsia could reduce bioavailability of nitric oxide through neutrophil autocrine function. Neutrophil-mediated endothelial cell injury was significantly greater in women with preeclampsia than in the other 2 groups. Hydrogen peroxide was important in neutrophil-mediated endothelial cell injury in preeclampsia as catalase inhibited endothelial cell injury. When neutrophils were pretreated with N G -nitro-Larginine methyl ester, neutrophil-mediated endothelial cell injury in preeclampsia was decreased, indicating a role for peroxynitrite formation as a mechanism of endothelial cell injury. In conclusion, the modulation of neutrophils causing superoxide production to dominate over nitrite release provides a reasonable explanation for endothelial cell dysfunction in preeclampsia. Key Words: endothelium Ⅲ free radicals Ⅲ neutrophils Ⅲ nitric oxide Ⅲ preeclampsia Ⅲ pregnancy P reeclampsia is a hypertensive disorder of human pregnancy and a leading cause of maternal and fetal morbidity and mortality. 1 There is increasing evidence to suggest endothelial cell damage and dysfunction in the pathogenesis of preeclampsia. 2 Although the actual cause of this endothelial damage is not well-known, neutrophils, through their ability to produce reactive oxygen species (ROS), have been implicated as likely candidates. 3 Superoxide anions (O 2 Ϫ ) have been shown to influence vascular tone either indirectly, by inactivating NO 4 and reducing the release of prostacyclin, 5 or by directly contracting smooth muscle. 6 High concentrations of superoxide have been found to reorient the arachidonic acid pathway in cells toward the production of thromboxane A2, which is a potent stimulator of vasoconstriction and platelet aggregation. 7 The imbalance between prostacyclin and thromboxane A2 is well-documented in preeclampsia. 8 Furthermore, neutrophil-derived superoxide anions can damage vascular integrity and endothelial cell function. 9 In preeclampsia, we...
Recently, numerous studies have identified that immature cell populations including stem cells and progenitor cells can be found among “side-population” (SP) cells. Although SP cells isolated from some adult tissues have been reported elsewhere, isolation and characterization of human trophoblast SP remained to be reported. In this study, HTR-8/SVneo cells and human primary villous cytotrophoblasts (vCTBs) were stained with Hoechst 33342 and SP and non-SP (NSP) fractions were isolated using a cell sorter. A small population of SP cells was identified in HTR-8/SVneo cells and in vCTBs. SP cells expressed several vCTB-specific markers and failed to express syncytiotrophoblast (STB) or extravillous cytotrophopblast (EVT)-specific differentiation markers. SP cells formed colonies and proliferated on mouse embryonic fibroblast (MEF) feeder cells or in MEF conditioned medium supplemented with heparin/FGF2, and they also showed long-term repopulating property. SP cells could differentiate into both STB and EVT cell lineages and expressed several differentiation markers. Microarray analysis revealed that IL7R and IL1R2 were exclusively expressed in SP cells and not in NSP cells. vCTB cells sorted as positive for both IL7R and IL1R2 failed to express trophoblast differentiation markers and spontaneously differentiated into both STB and EVT in basal medium. These features shown by the SP cells suggested that IL7R and IL1R2 are available as markers to detect the SP cells and that vCTB progenitor cells and trophoblast stem cells were involved in the SP cell population.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.